As indicated previously, the hippocampus is believed to be crucial for conscious recollection, a process that entails the re-experiencing and recall of an event and its associated details. Clinically, recollection is crucial for tests such as free recall and those that require the retrieval of associative information, such as where and when an event was experienced. The hippocampus is not required for memory that is based solely on familiarity. In contrast to recollection, familiarity–based memory is less detailed and usually involves remembering that an object or item has been encountered before, but without necessarily being able to recall anything else about it. Recognition tasks that require decisions based on matching memory to present information can be successfully completed with familiarity-based assessments.

Recollection impairments are present after stroke in the MTL due to, for example, hemorrhage or occlusion of the vascular supply to the hippocampus (involving the anterior and temporal artery, and to a lesser degree the anterior choroidal artery). Most strokes involving the hippocampus and MTL are ischemic; hemorrhages isolated to the hippocampus are uncommon and those in the temporal lobe are usually more lateral. Typical causes would be amyloid angiopathy or rupture of a middle cerebral artery aneurysm into the adjacent temporal lobe. Ott and Saver [27] reported cases of hippocampal lesions from strokes that were sufficient to induce amnesia (see Fig. 9.2 for a representative computed tomography [CT] scan of such a case).

Other investigations [24] have examined memory performance of patients who suffered from mild hypoxic ischemic encephalopathy, which is a form of transient global brain injury. Although diffuse brain regions can be affected, hypoxic ischemic encephalopathy can also selectively damage the hippocampus. Compared to healthy control participants, these patients showed memory impairment on recall and recognition memory tests; however, their recall deficit was significantly greater than their recognition deficit. Experimental measures designed to dissociate recollection from familiarity identified a selective recollection deficit in these patients [28, 29].

In 2004, Mayes and colleagues [30] described patient YR, who suffered an ischemic stroke that selectively affected both hippocampi. Consistent with the previously mentioned findings [28, 29], YR’s primary deficit reflected a loss of hippocampus-dependent memory. Her short-term, implicit and semantic memories, as well as familiarity-based recognition memory, were all spared. Her performance on tests that required recollection, such as free recall and paired-associate learning, however, was impaired.

Many of the studies that have reported anterograde amnesia after hippocampal damage also demonstrated deficits in the patients’ ability to recall details from past personal experiences (e.g., describe the first day of a job) [31]. These findings suggest that memory loss following hippocampal strokes extend to events of the distant past (retrograde amnesia). Further evidence of retrograde amnesia comes from a study that tested 20 patients with unilateral strokes, including patients who sustained damage to the hippocampus [32]. The patients were given tests of autobiographical memory in which they were asked to describe personal events from three remote time periods. They were also given tests of public events in which they answered questions about well-known events from different decades (e.g., “Who was the first person to set foot on the moon?”). The patients with hippocampal damage generated fewer details and had poorer recall of past personal events, particularly those from remote times. They also answered fewer correct responses to questions about well-known public events compared to their matched counterparts.

While recollection-specific deficits are a cardinal feature of hippocampal damage due to stroke, for example, familiarity-based memory impairment can supplement these deficits if the lesions are accompanied by damage to other MTL structures, namely the entorhinal, perirhinal, and the parahippocampal cortices. In their review, Aggleton and Shaw [33] reported, that, while focal hippocampal lesions selectively disrupt free recall (recollection), damage that extends beyond the hippocampus into other MTL regions results in recall and recognition deficits (also see [18]; but see [34] for a different view of recollection and familiarity).

Conventional laterality-specific functions are represented in the hippocampus. The left hippocampus is involved predominately in verbal episodic memory tasks whereas the right hippocampus is involved more in nonverbal episodic memory tasks, including the encoding and retrieval of spatial relations and location information. For example, poor verbal memory, as measured by story recall and tests that assess memory for a previously learned list of unrelated words, is associated with left hemisphere strokes [35]. Patients with ischemic right posterior hippocampal lesions present with relatively intact verbal memory, but have a specific impairment in nonverbal and spatial memory [36]. Szabo and colleagues [29] studied more than 50 patients using a neuropsychological battery that included a list-learning task, an auditory learning task, and tests of nonverbal memory, such as the Rey-Osterreith complex figure test. Strokes affecting the left hippocampus resulted in worse performance on the verbal memory tests (e.g., list-learning test) when tested at both short and long delays, and better performance on nonverbal memory tests (e.g., the Rey-Osterreith complex figure test). In contrast, strokes affecting right hippocampal regions resulted in the opposite pattern: poorer nonverbal than verbal memory.

The hippocampus is integral for the formation and recall of episodic memories, irrespective of when they are acquired. When the hippocampus is damaged as part of stroke-induced pathology, both anterograde and retrograde amnesia are experienced, as they are in other disease processes. If hippocampal lesions from stroke are accompanied by damage to additional regions of the MTL, familiarity-based recognition memory is also likely to be affected. Finally, the pattern of impairment from hippocampal strokes is dependent on the side of damage. Left-sided damage results in verbal memory impairments and right-sided damage results in nonverbal impairments.